Excessive salt intake is a contributing factor to the etiology of hypertension in man. In rodents excessive salt intake leads directly to hypertension. This unequivocal linkage has resulted in the use of rats as model preparations for the study of experimental hypertension. Prior experience, genetic factors, and deprivation state influence the amount of salt (NaC1) an organism consumes. changes in intake may reflect changes in the taste of salt mediated by the peripheral gustatory apparatus. Salt intake is also influenced by peripheral metabolic processes mediated by the liver, kidney and adrenal glands. Both neural and hormonal factors are intimately involved in sodium metabolism and regulation. We intend to assess the role of prior experience with salt in the development of salt preference and hypertension in the normal rat and in a strain of rats that is genetically susceptible to hypertension. We also intend to determine whether recently discovered changes in salt taste sensitivity as measured with neurophysiological techniques are causally related to changes in salt intake. And finally, this research will assess the role of area postrema and the nucleus of the solitary tract in control of fluid and electrolyte status, and blood pressure in rats.